Pulmonary Surfactant: A Unique Biomaterial with Life-saving Therapeutic Applications

Pioselli, Barbara; Salomone, Fabrizio; Mazzola, Giuseppe; Amidani, Davide; Sgarbi, Elisa; Amadei, Francesco; Murgia, Xabi; Catinella, Silvia; Villetti, Gino; Luca, Danièle De; Carnielli, Virgilio P.; Civelli, Maurizio

doi:10.2174/0929867328666210825110421

Cited by 12 publications

(9 citation statements)

References 499 publications

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“…Alveolar surfactants play a role in reducing alveolar surface tension and maintaining lung compliance ( 78 ). The membrane tension generated by alveolar swelling activates Piezo1 in alveolar type I epithelial cells (AT I), and the Piezo1-mediated rise in Ca 2+ activates pannexin hemichannels and leads to ATP release.…”

Section: Piezo1 Channel-mediated Chronic Inflammationmentioning

confidence: 99%

Piezo1 Channels as Force Sensors in Mechanical Force-Related Chronic Inflammation

Liu

Zheng

et al. 2022

Front. Immunol.

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Mechanical damage is one of the predisposing factors of inflammation, and it runs through the entire inflammatory pathological process. Repeated or persistent damaging mechanical irritation leads to chronic inflammatory diseases. The mechanism of how mechanical forces induce inflammation is not fully understood. Piezo1 is a newly discovered mechanically sensitive ion channel. The Piezo1 channel opens in response to mechanical stimuli, transducing mechanical signals into an inflammatory cascade in the cell leading to tissue inflammation. A large amount of evidence shows that Piezo1 plays a vital role in the occurrence and progression of chronic inflammatory diseases. This mini-review briefly presents new evidence that Piezo1 responds to different mechanical stresses to trigger inflammation in various tissues. The discovery of Piezo1 provides new insights for the treatment of chronic inflammatory diseases related to mechanical stress. Inhibiting the transduction of damaging mechanical signals into inflammatory signals can inhibit inflammation and improve the outcome of inflammation at an early stage. The pharmacology of Piezo1 has shown bright prospects. The development of tissue-specific Piezo1 drugs for clinical use may be a new target for treating chronic inflammation.

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Section: Piezo1 Channel-mediated Chronic Inflammationmentioning

confidence: 99%

Piezo1 Channels as Force Sensors in Mechanical Force-Related Chronic Inflammation

Liu

Zheng

et al. 2022

Front. Immunol.

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“…PS is a lipoprotein complex that lines the alveoli and decreases the surface tension to prevent lung atelectasis, and plays an important role in maintaining normal pulmonary function. The endogenous PS deficiency contributes to the lung dysfunction associated with ALI/ARDS [ 25 ]. A large number of in vitro data and in vivo animal studies have demonstrated that PS not only maintains bronchiolar patency during biophysical functions, but also protects of the lungs from the injury and infection of inhaled particles and microorganisms [ 25 ].…”

Section: Discussionmentioning

confidence: 99%

Sp1 mediated the inhibitory effect of glutamate on pulmonary surfactant synthesis

Li,

Fu,

Shi

et al. 2023

PLoS ONE

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Background Studies have shown that the release of endogenous glutamate (Glu) participates in lung injury by activating N-methyl-D-aspartate receptor (NMDAR), but the mechanism is still unclear. This study was to investigate the effects and related mechanisms of Glu on the lipid synthesis of pulmonary surfactant (PS) in isolated rat lung tissues. Methods The cultured lung tissues of adult SD rats were treated with Glu. The amount of [3H]-choline incorporation into phosphatidylcholine (PC) was detected. RT-PCR and Western blot were used to detect the changes of mRNA and protein expression of cytidine triphosphate: phosphocholine cytidylyltransferase alpha (CCTα), a key regulatory enzyme in PC biosynthesis. Western blot was used to detect the expression of NMDAR1, which is a functional subunit of NMDAR. Specific protein 1 (Sp1) expression plasmids were used. After transfected with Sp1 expression plasmids, the mRNA and protein levels of CCTα were detected by RT-PCR and Western blot in A549 cells. After treated with NMDA and MK-801, the mRNA and protein levels of Sp1 were detected by RT-PCR and Western blot in A549 cells. Results Glu decreased the incorporation of [3H]-choline into PC in a concentration- and time- dependent manner. Glu treatment significantly reduced the mRNA and protein levels of CCTα in lungs. Glu treatment up-regulated NMDAR1 protein expression, and the NMDAR blocker MK-801 could partially reverse the reduction of [3H]-choline incorporation induced by Glu (10−4 mol/L) in lungs. After transfected with Sp1 plasmid for 30 h, the mRNA and protein expression levels of CCTα were increased and the protein expression of Sp1 was also up-regulated. After A549 cells were treated with NMDA, the level of Sp1 mRNA did not change significantly, but the expression of nucleus protein in Sp1 was significantly decreased, while the expression of cytoplasmic protein was significantly increased. However, MK-801could reverse these changes. Conclusions Glu reduced the biosynthesis of the main lipid PC in PS and inhibited CCTα expression by activating NMDAR, which were mediated by the inhibition of the nuclear translocation of Sp1 and the promoter activity of CCTα. In conclusion, NMDAR-mediated Glu toxicity leading to impaired PS synthesis may be a potential pathogenesis of lung injury.

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“…First, progress in the understanding of surfactant function and dysfunction and our understanding of disease development and progression will improve targeted exogenous surfactant approaches. Second, improved surfactant nebulization methods developed in recent years will allow for early and less-invasive application, before ARDS is fully established. ,,− This would have the potential to curtail the progress of multiorgan injury, the major cause of mortality, on an individualized basis. − Third, the development of more synthetic preparations can be optimized for specific applications such as delivering other therapeutics such as anti-inflammatory agents on an individualized basis. ,, …”

Section: What Do Physiological and Pathophysiological Studies Teach U...mentioning

confidence: 99%

“…615−617 such as anti-inflammatory agents on an individualized basis. 66,520,618 8.2.5. Surfactant Composition across Mammalian Species.…”

Section: 541mentioning

confidence: 99%

Pulmonary Surfactant: A Mighty Thin Film

Possmayer,

Zuo,

Veldhuizen

et al. 2023

Chem. Rev.

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Pulmonary surfactant is a critical component of lung function in healthy individuals. It functions in part by lowering surface tension in the alveoli, thereby allowing for breathing with minimal effort. The prevailing thinking is that low surface tension is attained by a compression-driven squeeze-out of unsaturated phospholipids during exhalation, forming a film enriched in saturated phospholipids that achieves surface tensions close to zero. A thorough review of past and recent literature suggests that the compression-driven squeeze-out mechanism may be erroneous. Here, we posit that a surfactant film enriched in saturated lipids is formed shortly after birth by an adsorptiondriven sorting process and that its composition does not change during normal breathing. We provide biophysical evidence for the rapid formation of an enriched film at high surfactant concentrations, facilitated by adsorption structures containing hydrophobic surfactant proteins. We examine biophysical evidence for and against the compressiondriven squeeze-out mechanism and propose a new model for surfactant function. The proposed model is tested against existing physiological and pathophysiological evidence in neonatal and adult lungs, leading to ideas for biophysical research, that should be addressed to establish the physiological relevance of this new perspective on the function of the mighty thin film that surfactant provides.

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Pulmonary Surfactant: A Unique Biomaterial with Life-saving Therapeutic Applications

Cited by 12 publications

References 499 publications

Piezo1 Channels as Force Sensors in Mechanical Force-Related Chronic Inflammation

Piezo1 Channels as Force Sensors in Mechanical Force-Related Chronic Inflammation

Sp1 mediated the inhibitory effect of glutamate on pulmonary surfactant synthesis

Pulmonary Surfactant: A Mighty Thin Film

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